Heart disorders Flashcards
we will cover normal heart function ischaemic heart function MI heart failure valvular heart disease
describe normal heart anatomy
there are 2 atrium 2 ventricles
what valve lies in between the left atrium and left ventricle
the mitral valve/ bi CUSPID
how does blood travel around the heart
deoxygenated blood enters the Vena cava into the right atrium the tricuspid valve opens and blood moves into the RV after the SL valve opens and blood is carried into the pulmonary artery to get oxygen oxygenated blood is passed into the LA and then LV into the aorta to flow around the body
what is diastole
the filling of the ventricles when the heart is relaxed
what is systole
when the heart is contracting forcing blood out of the ventricles
what are the three main vessels that supply oxygenated blood directly to the heart
right coronary artery left anterior descending artery circumflex artery
what are the branches of the left main coronary artery
the circumflex artery left anterior descending artery
where does the left main coronary artery branch from
the aorta
definition of ischaemic heart disease
a group of clinical syndromes( signs and symptoms) that relate to myocardial ischaemia
definiton of ischaemia
is cell injury resulting from hypoxia induced by reduced blood flow most commonly due to a mechanical arterial obstruction
how many people die of ischaemia per year
64000
what are the clinical manifesations of ischaemic heart disease
MI
angina
chronic ischaemic heart disease
sudden cardiac death
why have death rates fallen by ischameic heart disease
due to awareness/prevention
and diagnosis and treatment
what can people to to prevent ischaemic heart disease
diet and exercise and modifiable risk factors such as hypertension and diabetes
what medications can people use to lower cholesterol
statins
what treatment can people undergo to reduce the likelihood of death by ischaemic heart disease
drugs- statins
acute presentations- antioplasty, stenting etc
arrythmias- implantable defib
heart failure- ventricular assist devices
what are the risk factors of ischamic heart disease
smoking
obesity
hypertension
diabetes
age
dsylipidaemia
family history
higher risk in men > woman
what is dyslipidaemia
due to increased levels of LDL in the blood
how do we treat dyslipidaemia
with the use of statins
what is the pathogenesis of ischaemic heart disease
insufficient coronary perfusion –> cardiac hypoxia –> cell injury which is sustained –> myocardial cell death leading to MI
describe LAD obstruction
sudden death artery AKA widowmaker
anterior infartion
50% of cases
descirbe circumflex obstruction
lateral infarction
20% of cases
describe right coronary artery obstruction
interior infarction
30% of cases
can involve the posterior septum
what can happen in ischamic heart disease on a cellular level
can lead to a reduction in oxidative phosphrylation and therefore reduction of ATP
As ATP levels falls what three pathways can occur
- reduction in the Na+ pump
- increase in anaerobic respiation
- dettatchment of ribosomes
what happens when there is a reduction in the sodium pump
leads to influx of ca2+, H20 and Na+
efflux of K+
leading to endoplasmic reticulum swelling and loss of microvilli
what does an increase of anaerobic respiration lead to
decreased glycogen
increased lactic acid therefore low pH
clumping together of nuclear chromatin
what happens in ribosomes dettach
leading to decrease in protein synethesis
explain the three pathways that occur when there is reduction in oxidative phosphorylation in the cellular level of ischaemic heart disease

what is artherosclerosis
material build up in the arterial wall due to fatty deposits
what are risk factors for artherosclerosis
smoking and BP
what else is located near the artherosclerosis
macrophaged which can initiate an inflammatory response
what does the pre clinical phase include of atherosclerosis
normal artery leads to fatty streak –> fibrofatty plaque –> advanced vunerable plaque
what does the clinical phase of artherosclerosis include
aneurysm and rupture
occlusion by thrombus
critical stenosis
what are unstable angina and MI caused by
plaque rupture
what is the difference between angina and MI
there is no detectable cell damage in angina
what are the clinical features of angina pectoris
strangled chest
pain due to inflammatory mediator
pain can be behind restrosternal chest pain, radiationto the epigastric shoulders
precipitated by running, eating, exposure to cold or stress
what is stable angina
1-5 minutes relieved by GTN spray
what are the characterisrics of unstable angina
intense
lasts longer
less exertion
spontaneous at rest
progressive pain
what are symrpoms of unstable angina
pale and clammy
sweating
weak pulse
nausea and vomitting
breathlessness
how do we diagnose ischamic heart disease
clinical features- severity of pain
changes on ECG
cardia blood markers
what is the theory of seeing cardiac blood markers in the blood
proteins such as troponin are normally held in cardiomyocytes –> released when the myocyte is necrotic and released into the blood stream
what do we do if GTN spray doesnt work
Call 999
Reassure/comfortable position
Give oxygen
Sublingual GTN
No Intra muscular injections! As they are too slow, and risk of bleeding
Give aspirin 300mg- provide note for hospital admin
If pt is unconscious begin resuscitation
what about non symptomatic ischaemic heart disease pts
patients are vunerable for upto 4+ weeks following MI or sudden increase in angina symptoms
what do we not recommend for patients who had coronary artery bypass graft
antibiotic prophylaxis
what are complications of an MI
Impaired contractility
tissue necrosis
electrical instability
pericardial inflammation
6 results
what can be the issues with MI
stroke
cardiogenic shock
congenetive HF
cardiac tamponade
arrythmias
pericarditis
what is HF
an inability to pulp enough blood to meet metabolic demands of the body
symptoms of HF
fatigue
breathless ness
peripheral oedema
which mechanisms help the failing heart maintain function
increase contractility
cardiac hypertrophy
neurohumoral responses
describe neurohumoral responses
fluid overload
fluid retention to maintain
renin angiotensin system
low cardiac output
what is cardiac hypertropy characterised by
increased heart size and mass
increased protein synthesis
fibrosis
abnormal proteins
what is the ejection fraction
the proportion of the blood that is actually ejected from the ventricles
what is systolic dysfuction
decreased contraxctility and therefore the ejection function decreeases to less than <40%
heart failure with reduced ejection function HRrEF
what is the typical ejection fraction
55-70%
what do we DIASTOLIC dysfunction
heart cannot fill proeprly with blood
heart failure with preserved ejection fracture HFpEF
describe left heart failure
damage to the left ventricles or valve
can lead to
Congestion in the pulmonary circulation, stasis of blood in the LS and inadequate perfusion of organs
what are the symptoms of Left heart disease
Breathlessness
Oedema due to pulmonary congestion
systemic hypoperfusion (organ failure
describe right heart failure
Increased back pressure through the pulmonary and venous circulation
Therefore leg swells
Most people have a combination of both
how do people get right heart failure
from left heart failure or pulmonary issues
what are the different types of valvular heart diseases
fail to fully open eg stenosis
fail to fully close eg flow reversal
vegetations - infective nodules the formation of infective vegetations on the heart is called infective endocarditis
what does abnormal valve function
abnormal blood flow
clot formation
risk of infection
what is stenosis due to
chronic injury / rheumatic fever
what is the pathological cause of mitral stenosis
rheumatic valvular disease
what can left ventricular hypertrophy lead to
ischaemia
syncope
decompensated Congenitive heart failure
why can we get mitral regurgitation
Calcification of the valve ring
Fibrous scarring of the papillary muscle and tethering valve leaflets
The papillary muscle can also rupture
Infective endocarditis
how can we fix mitral regurgitation
valve replacement